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In the fascinating report by Locatelli and colleagues (1), the authors conjecture a possible association between left temporal lobe epileptic activity and cardiac asystole or bradycardia. The authors cite their own experience with 3 patients, as well as a review of the literature constituting 10 reports on 14 patients, all of whom underwent simultaneous video electroencephalography-electrocardiography. I would submit, however, that the leap from cortical stimulation studies, in which a cause-and-effect relation may be apparent, to a complex clinical situation with uncontrolled variables is hazardous. Sinus bradycardia and asystole, for example, are also observed relatively frequently in patients with obstructive sleep apnea (Figure). In these patients, bradycardia and asystole are considered to be the consequences of airway obstruction and hypoxemia (2). Guilleminault and colleagues (3), for example, observed sinus pauses from 2.5 to 13 seconds in 11% of 400 patients with obstructive sleep apnea. Zwillich and associates (4) observed bradycardia during 95% of apneas; these bradycardiac episodes became more severe as apnea length and oxyhemoglobin desaturation increased.